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Major Loss of the 28-kD Protein of Gap Junction in Proliferating Hepatocytes

Dermietzel, Rolf and Yancey, S. Barbara and Traub, Otto and Willecke, Kaus and Revel, Jean-Paul (1987) Major Loss of the 28-kD Protein of Gap Junction in Proliferating Hepatocytes. Journal of Cell Biology, 105 (4). pp. 1925-1934. ISSN 0021-9525. PMCID PMC2114657. doi:10.1083/jcb.105.4.1925. https://resolver.caltech.edu/CaltechAUTHORS:20120626-092722040

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Abstract

There is a reduction in the 28-kD gap junction protein detectable by immunofluorescence in livers of partially hepatectomized rats and in cultured hepatocytes stimulated to proliferate. By the coordinate use of antibodies directed to the hepatic junction protein (HJP28) and the use of a monoclonal antibody that recognizes bromodeoxyuridine (BrdU) incorporated into DNA, we have been able to study the relationship between detectable gap junction protein and cell division. Hepatocytes that label with BrdU in the regenerating liver and in cell culture show a significant reduction of HJP28. Cells that do not synthesize DNA, on the other hand, show normal levels and distribution of immunoreactive gap junction protein. We postulate that the quantitative changes in gap junction expression might play an important role in the control of proliferation in the liver.


Item Type:Article
Related URLs:
URLURL TypeDescription
http://dx.doi.org/10.1083/jcb.105.4.1925DOIArticle
http://jcb.rupress.org/content/105/4/1925PublisherArticle
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2114657/PubMed CentralArticle
Additional Information:© 1987 Rockefeller University Press. After the Initial Publication Period, RUP will grant to the public the non-exclusive right to copy, distribute, or display the Article under a Creative Commons Attribution-Noncommercial-Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode, or updates thereof. Published October 1, 1987. Received for publication 4 December 1986, and in revised form 4 June 1987. The authors are grateful to Dr. D. Paul (Frauenhofer Institut, Hannover) who provided the culture medium for the embryonic hepatocytes used in this investigation. This research was supported by grants of the Deutsche Forschungsgemeinschaft to R. Dermietzel (De. 292/2-1) and to K. Willecke (Wi.270/13), and by grants GM 06965, GM 35963, and RR 07003 from the National Institutes of Health, as well as by the Ruddock Fund.
Funders:
Funding AgencyGrant Number
Deutsche Forschungsgemeinschaft (DFG)De 292/2-1
Deutsche Forschungsgemeinschaft (DFG)Wi 270/13
NIHGM 06965
NIHGM 35963
NIHRR 07003
Caltech Albert Billings Ruddock ProfessorshipUNSPECIFIED
Issue or Number:4
PubMed Central ID:PMC2114657
DOI:10.1083/jcb.105.4.1925
Record Number:CaltechAUTHORS:20120626-092722040
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20120626-092722040
Official Citation:Major loss of the 28-kD protein of gap junction in proliferating hepatocytes. R Dermietzel, S B Yancey, O Traub, K Willecke, and J P Revel 105:1925-1934. doi:10.1083/jcb.105.4.1925
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:32082
Collection:CaltechAUTHORS
Deposited By: Ruth Sustaita
Deposited On:26 Jun 2012 19:04
Last Modified:09 Nov 2021 20:03

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